PubMed · 6226483
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D Stoermer, G Wolz. 1983. Cement burns.. https://doi.org/10.1111/j.1600-0536.1983.tb04443.x
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Intraperitoneal administration of the cytokine interleukin-1beta (IL-1beta) induces brain-mediated sickness symptoms that can be blocked by subdiaphragmatic vagotomy. Intraperitoneal IL-1beta also induces expression of the activation marker c-fos in vagal primary afferent neurons, suggesting that IL-1beta is a key component of vagally mediated immune-to-brain communication. The cellular sources of IL-1beta activating the vagus are unknown, but may reside in either blood or in the vagus nerve itself. We assayed IL-1beta protein after intraperitoneal endotoxin [lipopolysaccharide (LPS)] injection in abdominal vagus nerve, using both an ELISA and immunohistochemistry, and in blood plasma using ELISA. IL-1beta levels in abdominal vagus nerve increased by 45 min after LPS administration and were robust by 60 min. Plasma IL-1beta levels increased by 60 min, whereas little IL-1beta was detected in cervical vagus or sciatic nerve. IL-1beta-immunoreactivity (IR) was expressed in dendritic cells and macrophages within connective tissues associated with the abdominal vagus by 45 min after intraperitoneal LPS injection. By 60 min, some immune cells located within the nerve and vagal paraganglia also expressed IL-1beta-IR. Thus, intraperitoneal LPS induced IL-1beta protein within the vagus in a time-frame consistent with signaling of immune activation. These results suggest a novel mechanism by which IL-1beta may serve as a molecular link between the immune system and vagus nerve, and thus the CNS.
The spatial distribution of chewing lice (Bovicola ovis) on their hosts was examined in Polypay and Columbia ewes initially artificially infested on the midside or the neck. Densities of lice were determined at 69 body sites in eight body regions at approximately monthly intervals for 2 years. In the second year, half of the ewes were mated and lice were counted at 26 body sites on the resulting lambs. Polypay ewes had higher densities of lice than Columbias at most inspections but there was little effect of infestation point or mating on either numbers or the distribution of lice. During periods of high louse numbers densities were generally greatest on the sides or the back. Densities on the head were also high at times and peaked later than overall louse densities. Shearing markedly reduced density but increased the proportion of lice found on the neck, belly and lowleg sites. The distribution of lice on the lambs was similar to that on the ewes except that fewer lice were found on the head. Comparisons of lice per part with the numbers of lice extracted from clipped patches indicated that a sheep with wool bearing area of 1 m2 and a mean count of one louse per 10 cm fleece parting carried approximately 2000 lice. At most times of the year inspections for sheep lice should be concentrated on the sides and back, but in recently shorn sheep greater attention should be paid to the lower neck and ventral regions. Implications of the observed distributions of lice for the efficacy of chemical treatments are discussed.
The effect of the non-peptide selective tachykinin NK1 receptor antagonist SR140333 has been investigated on oedema formation and neutrophil accumulation induced by thermal injury (50 degrees C for 5 min), mustard oil, substance P, the tachykinin NK1 agonist GR73632, and interleukin-1beta in the abdominal skin of the anaesthetised rat. SR140333 significantly inhibited (120 nmol/kg i.v.) or prevented (240 nmol/kg i.v.) the early oedema formation (0-10 min) induced by thermal injury. However, a dosing strategy which blocked NK1 receptors for 5 h (SR140333, 240 nmol/kg i.v. + 240 nmol/kg s.c.) failed to influence neutrophil accumulation measured 5 h after thermal injury. Thus, the neurogenic component mediated by NK1 receptors is important to elicit the early oedema formation, but does not influence subsequent neutrophil accumulation. Topical application of mustard oil (2%), a neurogenic inflammation stimulant, caused NK1 receptor-mediated early neurogenic plasma extravasation, but did not induce cutaneous neutrophil accumulation over 5 h. Substance P and GR73632 at high doses (1 nmol/site) also failed to elicit neutrophil accumulation. Neutrophil accumulation induced by interleukin-1beta (0.03-3 pmol i.d.) was not affected by SR140333 pretreatment. In conclusion, despite an early pronounced tachykinin NK1 receptor-dependent oedema response after thermal injury, the results suggest that subsequent neutrophil accumulation is not mediated by NK1 receptors. Furthermore, we have not obtained any evidence to suggest that either endogenous or exogenous tachykinins can directly induce neutrophil accumulation in the rat cutaneous microvasculature.